Obesity, because it alters the relationship between the lungs, chest wall, and diaphragm, has been expected to alter respiratory function. We studied 43 massively obese but otherwise normal, nonsmoking, young adults with spirometry, lung volume measurement by nitrogen washout, and single-breath diffusing capacity for carbon monoxide (DLCO). Changes in respiratory function were of two types, those that changed in proportion to degree of obesity--expiratory reserve volume (ERV) and DLCO--and those that changed only with extreme obesity--vital capacity, total lung capacity, and maximal voluntary ventilation. When compared with commonly used predicting equations, we found that mean values of subjects grouped by degree of obesity were very close to predicted values, except in those with extreme obesity in whom weight (kg)/height (cm) exceeded 1.0. In 29 subjects who lost a mean of 56 kg, significant increases in vital capacity, ERV, and maximal voluntary ventilation were found, along with a significant decrease in DLCO. Because most subjects fell within the generally accepted 95% confidence limits for the predicted values, we concluded that obesity does not usually preclude use of usual predictors. An abnormal pulmonary function test value should be considered as caused by intrinsic lung disease and not by obesity, except in those with extreme obesity.

Twenty-nine subjects with occupational asbestos exposure and clinical asbestosis were examined with high-resolution computed tomography (HRCT) to determine its sensitivity, relative to that of conventional computed tomography (CT), for detection of benign asbestos-related disease. Thin-section HRCT scans were obtained at five discrete levels through the mid and lower thorax in both prone and supine positions. The same technique was used in 34 age-similar control patients. Parenchymal abnormalities were seen most frequently in the posterior portion of the lung bases in the asbestos-exposed subjects. HRCT prone scans enabled basal structural abnormalities to be reliably distinguished from gravity-related physiologic phenomena in 25 asbestos-exposed subjects. HRCT was more sensitive than CT in detection of both pleural and parenchymal fibrosis. In subjects with clinical asbestosis, HRCT demonstrated parenchymal abnormality in 96%, compared with 83% for CT. Similarly, pleural thickening was shown in 100% of subjects at HRCT, compared with 93% at CT. HRCT could be an important adjunct in the evaluation of asbestos-related pleuroparenchymal fibrosis. An HRCT study including prone scans is a sensitive, reliable means of detecting thoracic abnormalities in asbestos-exposed individuals.

The objective of this study was to determine if damage to the articular cartilage alone or articular cartilage plus subchondral bone of the distal medial femoral condyle of young, exercised horses resulted in the formation of subchondral cystic lesions. Twelve Quarter Horses (age 1-2 years), free of clinical and radiographic signs of osteochondrosis and lameness were used. In 6 horses (Group 1), a 15 times 1 mm linear full thickness defect in the articular cartilage was made arthroscopically on the weightbearing surface of the distal aspect of the medial femoral condyle. In the other 6 horses (Group 2), a 15 times 3 mm full thickness elliptical cartilage defect was made, followed by burring a 5 mm diameter, 4 mm deep hole into the subchondral bone. Three weeks after surgery, all horses were hand walked and trotted for 2 weeks and then exercised for 6 min daily, 5 days a week for the next 14 weeks on a treadmill. They were then turned onto a small paddock for 6 weeks (6 months total). The development of subchondral cystic lesions was determined using radiography. Bone activity in the femoral condyle was monitored with nuclear scintigraphy. All horses that developed subchondral cystic lesions radiographically were subjected to euthanasia for gross and histological examination of the lesions. No subchondral cystic lesions and no clinical abnormalities were detected in the horses in Group 1. Subchondral cystic lesions developed radiographically in 5 of 6 horses in (Group 2). Scintigraphic findings of horses with subchondral cystic lesions were inconsistent. Histological examination of lesions revealed variable quantities of fibrous connective tissue, fibrocartilage and bone, with evidence of bone remodelling adjacent to the subchondral cystic lesion. The results suggest that damage to articular cartilage plus subchondral bone, but not articular cartilage alone, of the distal medial femoral condyle may lead to the development of subchondral cystic lesions. These findings indicate that all subchondral cystic lesions in horses may not be osteochondrosis-type lesions and that trauma to weightbearing articular surfaces of young horses may be a predisposing factor.

Asbestos-exposed persons with normal chest radiographs can demonstrate parenchymal abnormalities on high resolution computed tomography (HRCT). We reviewed the HRCT, clinical presentation, and results of pulmonary function tests in 169 asbestos-exposed workers with normal chest radiographs (ILO less than 1/0). The HRCT was normal or near normal in 76 subjects (Group 1), abnormal but indeterminate for asbestosis in 36, and abnormal and suggestive of asbestosis in 57 (Group 2). The indeterminate subjects were excluded from further analysis. The subjects in Groups 1 and 2 were not significantly different in their duration of asbestos exposure, latency, smoking history, or in measurements of airflow obstruction (FEV1/FVC% and %FEV1). Both the vital capacity percent predicted and diffusing capacity percent predicted were significantly lower in the abnormal subjects (Group 2) than in the normal subjects (Group 1) (79.0 versus 86.2, p = 0.005; 78.2 versus 87.1, p = 0.024; independent t test). We conclude that in asbestos-exposed subjects with normal chest radiographs, HRCT can identify a group of subjects with significantly reduced lung function indicative of restrictive lung disease when compared with a group with normal or near-normal HRCT.